Central effect of atrial natriuretic polypeptide on angiotensin II-stimulated vasopressin secretion in concious rats

Yamada, Takayuki; Nakao, Kazuwa; Morii, Narito; Itoh, Hiroshi; Shiono, Satoshi; Sakamoto, Makoto; Sugawara, Akira; Saito, Yoshihiko; Ohno, Hideto; Kanai, Akira; Katsuura, Goro; Eigyo, Masami; Matsushita, Akira; Imura, Hiroo

doi:10.1016/0014-2999(86)90802-2

Cited by 95 publications

(24 citation statements)

References 9 publications

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“…Our observation that the intravenous ANP infusion inhibited ANG II-induced increase in plasma AVP levels was in agreement with previous studies demonstrating that the intraventricular administration of ANP inhibited the increase in blood pressure and AVP secretion induced by ANG II central administration (3,12,26,32). However, it is not known whether or not circulating ANP inhibits the induction of AVP secretion by ANG II.…”

Section: Simultaneous Infusion Of Anp Inhibits Ang Ii-induced Elevatesupporting

confidence: 82%

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

Matsukawa

Miyamoto

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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.2010.-We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg Ϫ1 ·min Ϫ1 ) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg Ϫ1 ·min Ϫ1 ) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg Ϫ1 ·min Ϫ1 ) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II. atrial natriuretic peptide; baroreceptor reflex; blood pressure; vasopressin ANGIOTENSIN II (ANG II) and atrial natriuretic peptide (ANP) are known to be important regulators of the fluid balance and arterial pressure (12,22,23), and an interaction between ANG II and ANP has been observed in several organs involved in the central nervous system (12,26). The intracerebroventricular administration of ANG II was recently shown to produce increased arterial pressure with elevated secretion of arginine vasopressin (AVP) (22,23). In addition, the intracerebroventricular administration of ANP inhibited the increase in both blood pressure and AVP secretion induced by the central administration of ANG II (2,8,22,27). It was suggested that circulating ANG II can stimulate AVP secretion in addition to exerting a potent pressor effect (22,23,30). However, it is still uncertain whether circulating ANP inhibits the response of AVP to circulating ANG II.In the present study, we investigated the effect of intravenous ANP infusion on the response of plasma AVP levels to intravenously infused ANG II in humans. Because the secretion of AVP is known to be inhibited by stimulation of the baroreceptors (11, 27), the pressor effect of ANG II may counteract its direct action of promoting AVP secretion. Thus, we evaluated the interaction between ANG II and ANP on AVP secretion while the elevations in arterial pressure and central venous pressure produced by ANG II were inhibited by simultaneous infusion of nitroprusside. SUBJECTS AND METHODS SubjectsWe evaluated eight healthy male volunteers (42 Ϯ 1 yr, mean age Ϯ SE). All subjects were within 10% of their ideal body weight and were determined to be free from endocrine, me...

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Section: Simultaneous Infusion Of Anp Inhibits Ang Ii-induced Elevatesupporting

confidence: 82%

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

Matsukawa

Miyamoto

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Pulmonary capillary wedge pressure, pulmonary arterial pressure, and right atrial pressure were determined with a Swan-Ganz catheter ( Measurements of the plasma hormones. The plasma ANP concentration was measured by a specific RIA for a-ANP reported previously.9 31 32 Briefly, this RIA recognizes a carboxyterminal fragment of ANP, a-ANP (17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28), and the minimal detectable quantity of a-human ANP is 1 pg/tube. Plasma renin activity and the plasma aldosterone concentration were measured with commercially available kits, Renin RIA beads (Dainabot Co., Ltd., Tokyo, Japan) and Aldosterone Test Shionogi (Shionogi Co., Ltd., Osaka, Japan), which are based on previously reported methods.33 3 Plasma norepinephrine and epinephrine levels were measured by high-performance liquid chromatography combined with the trihydroxyindole fluorometric procedure.…”

Section: Methodsmentioning

confidence: 99%

Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function.

Saito¹,

Nakao²,

Nishimura³

et al. 1987

Circulation

326

167

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Synthetic a-human atrial natriuretic polypeptide was infused in patients with congestive heart failure (CHF) (New York Heart Association class III or IV) and in those without CHF. The infusion of atrial natriuretic polypeptide (ANP) at a rate of 0. 1 gg/kg/min significantly decreased pulmonary capillary wedge pressure and increased stroke volume index in all of the patients with CHF, whereas it decreased pulmonary capillary wedge pressure but caused no significant change in stroke volume index in the patients without CHF. Concomitant significant reductions in total systemic resistance were observed in both groups of patients. The ANP infusion significantly increased the urine volume, the excretion of sodium, and endogenous creatinine clearance in the patients without CHF. In the patients with CHF, it also showed a tendency to increase all these variables, but the urine volume did not correlate with the reduction in pulmonary capillary wedge pressure. The ANP infusion also decreased plasma aldosterone concentrations in these patients, although no significant difference was observed in the decrement of the plasma aldosterone concentration in the patients with and those without CHF. These findings indicate that the ANP infusion improves left ventricular function in patients with CHF, and suggest that this improvement results mainly from the vasodilating activity of ANP.Circulation 76, No. 1, 115-124, 1987. AFTER THE EPOCHAL discovery of the potent diuretic, natriuretic, and vasorelaxant activities in an extract from rat atria by de Bold et al. ,' multiple forms of natriuretic polypeptides with high and low molecular weights have been isolated fromn rat and human atria and implicated in the control of blood pressure, water, and electrolyte balance.2-1 Accumulating evidence indicates that a-atrial natriuretic polypeptide (a-ANP)

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“…Furthermore. ANP was found to attenuate AVP release produced by angiotensin I1 (12). In in vitro studies, moreover, ANP has been reported to stimulate AVP release in small doses, and in large doses, to attenuate the release of AVP (13).…”

mentioning

confidence: 97%

Effect of Atrial Natriuretic Peptide on the Vasopressin Response to Osmotic and Hemorrhagic Stimuli in Dogs

Inoue

Kimura

Ota

et al. 1990

J Neuroendocrinology

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Effect of atrial natriuretic peptide (ANP) on the vasopressin response to osmotic stimulation (Experiment I) as well as to hemorrhage (Experiment II) was investigated in anesthetized dogs. Moreover, cardiovascular function and renal water and electrolyte excretion were studied. In Experiment I , 2.5 M NaCI, containing 0.02 pg.kg ' of ANP, was infused intravenously at a rate of 0.2 ml.kg-'. min ' after one bolus injection of 0.75 pg.kg ' ANP (HSA group). In the control group, 2.5 M NaCl alone (HS group) was infused.The infusion was continued for 75 min. In Experiment 11, 0.15 M NaCI, containing the identical dose of ANP to Experiment I (HA group), or 0.15 M NaCl alone (H group) was infused intravenously during bleeding at a rate of 1 ml.kg-'.min ' for 40 min. In Experiment I, infused ANP suppressed the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and attenuated ANP release and a rise in arterial and central venous pressures in response to plasma volume expansion, without the enhanced natriuresis. In Experiment I I , infused ANP neither impaired t h e vasopressin response to bleeding nor potentiated a fall in mean arterial pressure and central venous pressure.In conclusion, ANP at physiological and/or supraphysiological range may suppress the vasopressin response to a mild osmotic stimulation, but not to a strong osmotic stimulation and to hemorrhage. In addition, ANP given intravenously may attenuate ANP release and a rise in blood pressure without any natriuresis.It has recently been postulated that there is a direct relationship between the release of atrial natriuretic peptide (ANP) and that of vasopressin (AVP), and this mutual relationship may be important in the regulation of body fluid.AVP has been reported to stimulate ANP release in in vivo and in vitw studies (1-3). On the contrary, the central and peripheral administrations of ANP have been shown to attenuate AVP release in euhydration as well as the AVP response to dehydration, hemorrhage and osmotic stimulation in animals (4-9) and human subjects (10. 1 I). Furthermore. ANP was found to attenuate AVP release produced by angiotensin I1 (12). In in vitro studies, moreover, ANP has been reported to stimulate AVP release in small doses, and in large doses, to attenuate the release of AVP (13).On the other hand, it has been documented that peripheral administration of ANP has no effect on AVP release in rats, sheep and man ( 5 , 14-18). Furthermore, AVP release has been shown to increase in response to hypertonic saline given iv. despite a marked rise in ANP release (1 9).Thus, it is still uncertain whether a rise in plasma ANP within physiological and/or supraphysiological range really affects AVP release in response to osmotic and hemorrhagic stimuli.In the present study, therefore, effects of ANP (iv) on AVP release elicited by hypertonic saline and hemorrhagic shock were investigated. Hypertonic saline infusion and continuous bleeding were carried out in ancsthetizcd dogs. In addition. renal water...

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Central effect of atrial natriuretic polypeptide on angiotensin II-stimulated vasopressin secretion in concious rats

Cited by 95 publications

References 9 publications

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function.

Effect of Atrial Natriuretic Peptide on the Vasopressin Response to Osmotic and Hemorrhagic Stimuli in Dogs

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